From Beyond The Rainbow Somewhere

Day: 06/02/2015

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Glaucoma is a disease of the optic nerve, which is the long “cable” that connects the cells that transmit all of the visual information from the retina to visual targets in the brain. Glaucoma is first and foremost an eye disease, and the initial damage to the optic nerve is thought to take place in the eye. However, because the optic nerve is part of the central nervous system, one can certainly think of glaucoma affecting the brain. It is more appropriate to say that glaucoma is a neurodegenerative disease of the eye, although there are some influences of the brain on glaucoma and vice versa. In this article we will discuss some of the ways in which the optic nerve and brain interact in glaucoma.

Can Pressure Inside the Brain Influence Glaucoma?

While one of the major risk factors of glaucoma is elevated eye pressure, more recently scientists have discovered that the pressure inside the brain may also influence glaucoma. This may be particularly true in patients who have “normal pressure glaucoma.” The rationale is that when the pressures inside the brain are lower than normal, and the pressures in the eye are “normal,” the difference between these two pressures (also called the translaminar pressure gradient) may still cause damage to the optic nerve.

Dr. Samuels’ research focuses on understanding which cells in the brain control eye pressure and brain pressure.

Dr. Fautsch is developing an animal model to study how lower brain pressures may influence optic nerve health and the development of glaucoma.

Dr. De Deyn is tackling this question from a different perspective. It has been known for some time that patients with Alzheimer’s disease may have changes in their optic nerves that mimic glaucoma. It is also known that Alzheimer’s patients have lower brain pressure. Dr. De Deyn’s team is studying the mechanisms by which patients with Alzheimer’s disease have increased risk of glaucoma. All of these studies will help shed light on the impact of brain pressure on the development and progression of glaucoma, in particular “normal pressure glaucoma.”

Indeed, perhaps in the future there will be treatments to influence brain pressure and thus glaucoma.

Do Changes in Retina Cells Affect the Brain?

Another area of active research is uncovering ways in which the degeneration of the retinal cells in glaucoma affects the visual pathways of the brain. Because the final step in neurodegeneration that causes glaucoma is death of the retinal ganglion cells of the optic nerve, it is perhaps not surprising that since these cells project all the way to the brain, that there would be changes in the cells of the brain as well.

Funded in part by BrightFocus Foundation, Dr. David Calkins and his team have uncovered some of the very early changes that occur in the brain in response to elevated eye pressure. These include decreased function of the retinal ganglion cells in their visual targets of the brain (Study 1 | Study 2).

Another team, funded by the BrightFocus Foundation and led by Dr. Kevin Chan, is developing new imaging techniques using MRI (magnetic resonance imaging) to study early changes in the visual system of the brain in glaucoma patients. They hope to uncover a noninvasive and comprehensive way to evaluate the effect of chronic high eye pressures on the structures of the brain involved in processing vision. A complete understanding of how the visual pathways are affected early in glaucoma neurodegeneration will help investigators identify new targets for treatment and better ways to detect glaucoma progression.

Glaucoma and Alzheimer’s: Is There a Connection?

Does glaucoma share any common degeneration pathways with other neurodegenerative diseases of the brain, such as Alzheimer’s disease? This is another area of active investigation and Dr. Stuart McKinnon, Dr. Ian Trounce, and Dr. John Wood have all contributed to this area.

Dr. McKinnon has published studies on the role of several abnormal proteins that are found in the brains of Alzheimer’s disease patients, including amyloid beta, on the retinal ganglion cells that die in glaucoma.

Dr. Trounce and his colleagues have studied another Alzheimer’s disease protein in more detail, specifically amyloid precursor protein. Their research focuses on the effect of age and elevated eye pressure on amyloid precursor protein breakdown and whether restoration of this protein may actually protect the optic nerve from injury.

Most recently, Dr. Wood was funded to study yet another Alzheimer’s disease protein, called tau. His work suggests that the characteristic changes in the tau protein that occur in Alzheimer’s disease, also occur in glaucoma.

All of these studies bring together what is known about the mechanisms underlying Alzheimer’s disease and applies it to glaucoma, in hopes of identifying new targets for treatment.

Summary

So, is glaucoma a brain disease? Certainly, glaucoma is a disease of the optic nerve, which can be considered an extension of the brain. And the optic nerve and brain influence each other in the neurodegenerative processes that results in glaucoma. By studying changes in the optic nerve and the brain, researchers will be advancing our understanding of glaucoma and developing new ways to diagnose, assess, and treat this potentially blinding disease.

Manger has dementia. Schoenfeld is her “surrogate decision maker” meaning that legally, she is the person who makes decisions about Manger’s health care. Schoenfeld says Chaparral House is the second nursing home where Manger has lived. The first was 45 minutes away, and Schoenfeld wasn’t able to visit as often.

At that first home, caregivers recommended antipsychotic sedatives for some of Manger’s behaviors, like crying out and outbursts. Schoenfeld wasn’t thrilled about the idea but agreed to it, thinking her aunt might get better care if staff members weren’t unhappy with her behavior.

Coming Out of a Fog

Two years later, Schoenfeld moved her aunt to Chaparral House to have her closer. By this time, Manger appeared to be in a fog. Eventually, Schoenfeld broached the idea of weaning her aunt from the medication. As soon as they did, she says things turned around.

“I could see her personality again, I was so happy,” Schoenfeld said. “My sister came to visit and (Aunt Lill) used my sister’s name and clearly recognized her, which we had not seen in the years that she was on the medication. I only wish I had done that sooner.”

Schoenfeld says it just didn’t feel right to have her aunt sedated. “If a baby is crying, I mean most people will go to a baby and comfort them. They won’t try to ignore them and drug them,” she says.

KJ Page, administrator of Chaparral House, shares that philosophy. Page says in many cases, dementia patients came to their facility with a prescription to be given antipsychotics half an hour before bath time. Then, a number of years ago, she read a book called Bathing Without a Battle about why it can be such a challenge to bathe dementia patients.

She asks people to imagine putting themselves in the place of the nursing home resident. “A person they didn’t know, couldn’t recognize, comes to take off their clothes,” she says. “Ah! No wonder they’re screaming and fighting and kicking!”

Page says after that “Aha!” moment, the staff came to a new agreement. The residents were not out running marathons or engaging in other sweat-inducing activities, so regular showers weren’t necessary. Instead, residents would have a regular caregiver do simple sponge baths.

Page says the results inspired further changes.

“It just rolled into what else are they fighting for, and why do we need to have a fight?” Page says, “What can we do to make it easier for people and the staff? And that’s how we approached it from there on.”

It worked. While Page says antipsychotics do have a place for some people, not one of Chaparral House’s dementia patients is currently taking the medications.

Grading Nursing Homes on Avoiding Antipsychotic Drugs

Chaparral House’s experience is unusual. In California nursing homes, just over 15% of dementia patients are on these drugs. That’s far more than advocates say is necessary. But that is actually down from almost 22% just 3 years ago. That’s when the federal government began regulating their use for dementia patients in nursing homes. This came in response to several studies warning the medicines had serious risks, including strokes, falls, and even death.

The new guidelines stipulate that nursing homes are graded on the percent of their dementia patients receiving antipsychotic medications. That figure becomes part of their rating on Nursing Home Compare, a tool from Medicare that helps consumers compare information about nursing homes.

The drugs are traditionally deployed to control what are seen as problem behaviors. Reducing the medication requires new approaches and retraining staff.

Caroline Stephens, assistant professor at the University of California – San Francisco School of Nursing, who specializes in psychiatric care for the elderly and long-term care policy, says that the new regulations have had a positive impact on staff. “They’re now realizing we don’t have to reach for the medication and they’re getting to think creatively about what we can do for this resident.”

Clinicians Become ‘Good Detectives’

As a consultant at the Hayward Healthcare and Wellness Center nursing home in Hayward, Calif., Stephens helps train nurses and staff on person-centered care, which means being attentive to the cues people give and trying to understand what is bothering them even if they can’t communicate it directly.

Stephens says the new regulations have given more credence to the approach. She describes one of her success stories in helping a dementia patient who was always fighting to leave the facility at the end of the day.

“They felt they needed to catch the bus, they had to get home because they need to take care of their daughter,” she says.

Instead of physically restraining the person or prescribing medication, Stephens says they put a sign on the door that said, simply, “It’s a holiday; buses aren’t running today.” The sign worked. The person stopped fighting to leave and there was no need for antipsychotic medication.

At another nursing home, Stephens consulted with staff about a resident who was disruptive and constantly wandered at night — including into other patients’ rooms. He had been given an antipsychotic to control his behavior. But in a deeper look at his background, staff learned that he’d worked as a night security guard for most of his adult life.

The staff came up with a new plan. They gave the resident a badge and clipboard and walked with him on an abbreviated set of “evening rounds.” Sure enough, he’d willingly go to bed after that and they were able to take him off medication.

Stephens says when the patients themselves can’t communicate, it’s vital to talk to family, to find out what the person did for a living and what they enjoyed in life.

“It is our job as clinicians to be good detectives,” she explains.

This is especially important as nursing homes serve an increasingly diverse clientele. Stephens says the nursing home model was built around an older, white, female patient. Today, the demographics have changed.

At Hayward Healthcare and Wellness, she says, “There are probably 15 different racial groups and a minimum of five languages spoken.”

Risk of Cherry-Picking Patients

One of the big advocates for the federal regulations was Tony Chicotel, staff attorney with California Advocates for Nursing Home Reform. He welcomes the guidelines but says he is concerned about an unintended consequence.

While across the state the overall rate of antipsychotic use has dropped, he says that several hundred nursing homes have rates that have either stayed the same or increased, in some cases almost doubled.

Chicotel says that in an effort to decrease their patients on antipsychotics to get better ratings, some facilities may be cherry-picking patients, essentially warehousing the hardest to wean from anti-psychotics in the bleakest facilities.

Chicotel says families and caregivers can look up a nursing home’s antipsychotic drug use rates as well as other drug usage data on websites, including Nursing Home Compare.

Still, these guidelines and ratings cover only nursing homes. Increasingly, Chicotel says, he is fielding calls from families worried about the use of antipsychotics in assisted living and home care settings, which aren’t covered by the regulations.

“We need to be more proactive about trying to get data for assisted living facilities and reconfiguring our message so it’s more applicable to assisted-living facilities,” Chicotel says.

Earlier this year, the GAO released a report urging HHS to expand its regulation of antipsychotics in dementia patients to settings besides nursing homes.

UCSF professor Stephens says this points to retraining ever more medical professionals in patient-centered care, eliminating the need for patients to be medicated as a form of restraint.

“If we can train generalists, I think we can make some headway,” she says.

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The US space agency plans to try out the largest parachute ever deployed Wednesday during a flying saucer launch that will test new technologies for landing on Mars.

The test flight of the flying saucer, known as the Low-Density Supersonic Decelerator, will be broadcast live on NASA’s website beginning at 1:30 pm (1730 GMT).

Since the atmosphere on Mars is so thin, any parachute that helps a heavy, fast-moving spacecraft touch down needs to be extra strong.

The US space agency figured out how to do this decades ago, beginning with the Viking mission which put two landers on Mars in 1976.

But with the goal of sending humans to Mars in the 2030s, the agency is now testing a more advanced, new generation of parachute technology, known as the Supersonic Ringsail Parachute, that could allow even heavier spacecraft—the kind that may have humans and months of food and supplies on board—to land softly.

“We want to see if the chute can successfully deploy and decelerate the test vehicle while it is in supersonic flight,” NASA’s Jet Propulsion Laboratory said in a statement.

The test vehicle weighs 6,808 pounds (3,088 kilograms), or about twice the weight of the kind of robotic rover spacecraft NASA is currently capable of landing safely on Mars.

The parachute, described by NASA JPL as “the largest parachute ever deployed,” is 100 feet (30 meters) in diameter.

The goal is for the chute to “slow the entry vehicle from Mach 2 to subsonic speeds,” NASA said.

The test will involve sending the saucer, an inner-tube shaped decelerator and parachute to an altitude of 120,000 feet (37 kilometers) over the Pacific Ocean with the help of a giant balloon.

The balloon will release the spacecraft and rockets will lift the vehicle even higher, to 180,000 feet (55 kilometers), reaching supersonic speeds.

“Traveling at three times the speed of sound, the saucer’s decelerator will inflate, slowing the vehicle, and then a parachute will deploy at 2.35 times the speed of sound to carry it to the ocean’s surface,” NASA said.

The first test flight of the flying saucer was in June 2014, and another test flight is planned in 2016.

A different kind of parachute known as the Supersonic Disksail was tested in the 2014 flight but it did not inflate as hoped, and shredded to pieces at the high speed and altitude.

NASA said researchers have since “gained significant insight into the fundamental physics of parachute inflation,” and the team “has been re-writing the book on high speed parachute operations” since last year, the agency said.

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On Sunday, May 31, 2015, NASA’s Cassini spacecraft made its latest and final flyby of Hyperion, Saturn’s spongy moon. At around 9:36 a.m. EDT Cassini came within 21,000 miles (34,000 km) of Hyperion’s surface — not its closest approach ever but certainly close enough to grab some fantastic images of this porous and punched-in world.

The image above is a color composite made from images acquired in optical wavelengths (i.e., Cassini’s red, green, and blue color filters) with some contrast enhancement and a bit of color saturation boosting as well. This is about what Hyperion would look like to an astronaut’s eyes, if she happened to have been riding along with Cassini last Sunday.

At 255 x 163 x 137 miles (410 x 262 x 220 kilometers), Hyperion is the largest of Saturn’s irregularly-shaped moons and its eighth-largest overall. Scientists think it could be what’s left over from a larger moon that was blown apart in the distant past.

Because of its porosity and low density, impacts on Hyperion tend to create punched-in craters with little to no ejecta, giving it its strange spongelike appearance.

Discovered in 1848 Hyperion is four times as far from Saturn as our moon is from us yet completes an orbit every 21 days, getting gravitational tugs and nudges from its inner neighbor Titan as it passes.

In fact some of Hyperion’s reddish coloration may come from Titan, as hydrocarbons from its atmosphere get blown into orbit by the solar wind and eventually fall on Hyperion, where they concentrate in low spots and impact craters.

Cassini will not come this close to Hyperion again for the remainder of its mission, which will come to an end in September 2017 when it makes a final dive between the rings and down into Saturn’s atmosphere.

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Implications profound for neurological diseases from autism to Alzheimer’s to multiple sclerosis.

In a stunning discovery that overturns decades of textbook teaching, researchers at the University of Virginia School of Medicine have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. That such vessels could have escaped detection when the lymphatic system has been so thoroughly mapped throughout the body is surprising on its own, but the true significance of the discovery lies in the effects it could have on the study and treatment of neurological diseases ranging from autism to Alzheimer’s disease to multiple sclerosis.

“Instead of asking, ‘How do we study the immune response of the brain?’ ‘Why do multiple sclerosis patients have the immune attacks?’ now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels,” said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA’s Center for Brain Immunology and Glia (BIG). “It changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can’t be studied. But now we can ask mechanistic questions.”

“We believe that for every neurological disease that has an immune component to it, these vessels may play a major role,” Kipnis said. “Hard to imagine that these vessels would not be involved in a [neurological] disease with an immune component.”

New Discovery in Human Body

Kevin Lee, PhD, chairman of the UVA Department of Neuroscience, described his reaction to the discovery by Kipnis’ lab: “The first time these guys showed me the basic result, I just said one sentence: ‘They’ll have to change the textbooks.’ There has never been a lymphatic system for the central nervous system, and it was very clear from that first singular observation – and they’ve done many studies since then to bolster the finding – that it will fundamentally change the way people look at the central nervous system’s relationship with the immune system.”

Even Kipnis was skeptical initially. “I really did not believe there are structures in the body that we are not aware of. I thought the body was mapped,” he said. “I thought that these discoveries ended somewhere around the middle of the last century. But apparently they have not.”

‘Very Well Hidden’

The discovery was made possible by the work of Antoine Louveau, PhD, a postdoctoral fellow in Kipnis’ lab. The vessels were detected after Louveau developed a method to mount a mouse’s meninges – the membranes covering the brain – on a single slide so that they could be examined as a whole. “It was fairly easy, actually,” he said. “There was one trick: We fixed the meninges within the skullcap, so that the tissue is secured in its physiological condition, and then we dissected it. If we had done it the other way around, it wouldn’t have worked.”

After noticing vessel-like patterns in the distribution of immune cells on his slides, he tested for lymphatic vessels and there they were. The impossible existed. The soft-spoken Louveau recalled the moment: “I called Jony [Kipnis] to the microscope and I said, ‘I think we have something.’”

As to how the brain’s lymphatic vessels managed to escape notice all this time, Kipnis described them as “very well hidden” and noted that they follow a major blood vessel down into the sinuses, an area difficult to image. “It’s so close to the blood vessel, you just miss it,” he said. “If you don’t know what you’re after, you just miss it.”

“Live imaging of these vessels was crucial to demonstrate their function, and it would not be possible without collaboration with Tajie Harris,” Kipnis noted. Harris, a PhD, is an assistant professor of neuroscience and a member of the BIG center. Kipnis also saluted the “phenomenal” surgical skills of Igor Smirnov, a research associate in the Kipnis lab whose work was critical to the imaging success of the study.

Alzheimer’s, Autism, MS and Beyond

The unexpected presence of the lymphatic vessels raises a tremendous number of questions that now need answers, both about the workings of the brain and the diseases that plague it. For example, take Alzheimer’s disease. “In Alzheimer’s, there are accumulations of big protein chunks in the brain,” Kipnis said. “We think they may be accumulating in the brain because they’re not being efficiently removed by these vessels.” He noted that the vessels look different with age, so the role they play in aging is another avenue to explore. And there’s an enormous array of other neurological diseases, from autism to multiple sclerosis, that must be reconsidered in light of the presence of something science insisted did not exist.

About this neuroscience research

The findings have been published online by the prestigious journal Nature and will appear in a forthcoming print edition. The article was authored by Louveau, Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Lee, Harris and Kipnis.

Funding: The study was funded by National Institutes of Health grants R01AG034113 and R01NS061973. Louveau was a fellow of Fondation pour la Recherche Medicale.

Structural and functional features of central nervous system lymphatic vessels

One of the characteristics of the central nervous system is the lack of a classical lymphatic drainage system. Although it is now accepted that the central nervous system undergoes constant immune surveillance that takes place within the meningeal compartment1, 2, 3, the mechanisms governing the entrance and exit of immune cells from the central nervous system remain poorly understood4, 5, 6. In searching for T-cell gateways into and out of the meninges, we discovered functional lymphatic vessels lining the dural sinuses. These structures express all of the molecular hallmarks of lymphatic endothelial cells, are able to carry both fluid and immune cells from the cerebrospinal fluid, and are connected to the deep cervical lymph nodes. The unique location of these vessels may have impeded their discovery to date, thereby contributing to the long-held concept of the absence of lymphatic vasculature in the central nervous system. The discovery of the central nervous system lymphatic system may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.

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New research reveals what factors into the relationship between having nightmares and psychotic experiences.

The term parasomnia is one experts use to classify sleep abnormalities and disorders, such as nightmares, night terrors, and sleepwalking. And according to a new study published in theBritish Journal of Psychiatry, children who experience parasomnias may experience psychotic symptoms when they grow older.

“We have previously demonstrated a cross-sectional relationship between the presence of nightmares and night terrors and psychotic experiences at age 12,” researchers wrote. “However, it is essential to determine whether parasomnias are possible precursors of psychotic experiences using longitudinal data. Therefore, we examined the relationship between the most common parasomnias in childhood…to later psychotic experiences reported at 18 years using data from a large UK birth cohort.”

The cohort is the Avon Longitudinal Study of Parents and Children, which began in order to see what factors into development, health, and disease during childhood. The present study culls the cohort’s parental reports and participant interviews to assess individuals’ experience with nightmares at certain ages throughout the study: between ages 2 and 9; age 12; and age 18.

The results showed those who have nightmares and night terrors at age 12 are more likely to experience psychotic symptoms at age 18. However, this link was influenced by cofounding variables, such as age, mood, family history, as well as baseline psychotic experiences at age 12.

“The presence of anxiety and depressive symptoms as confounding factors in those with sleep disturbance could potentially explain the findings,” Dr. Andrew Thompson, lead study author from Warwick Medical School, said in press release. “Experience of stressful events has also been related to both the development of both nightmares and psychotic symptoms in late childhood and may be important.”

While this confirms the prior study’s finding of a relationship between nightmares, night terrors, and psychotic symptoms, it doesn’t speak to sleepwalking. And in this study, the relationship with night terrors wasn’t as strong. Even so, researchers conclude these findings “suggest that specific parasomnias … are a potential risk indicator for the development of … psychotic experiences.”

The National Sleep Foundation reported parasomnias often run in the family, and there may be a genetic factor in many cases. Brain disorders, too, influence parasomnias, as do other sleep disorders, such as obstructive sleep apnea.

But for some, parasomnias can be improved just by adopting healthy sleep habits. Maintaining a regular schedule, managing stress, and getting the recommended amount of sleep can control symptoms. Drug therapies are also available.

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A group of students from Yale’s Department of Molecular Physics and Biochemistry traveled to Ecuador and found a fungus that wants to eat polyurethane. This new type of fungus can digest polyurethane in two weeks, rather than the 1,000 years it would take just sitting around.

It’s the first fungus ever found to survive on only polyurethane, no oxygen needed, which is why they want to use it at the bottom of landfills.

The fungus is called Pestalotiopsis microspora and is assumed to work by releasing a serine hydrolase, which degrades the polyurethane. It functions equally as well under water, so we may be able to clean the oceans with them.

Since the discovery, researchers have found that they can degrade the plastic and it will not retain any toxicity. It can actually be eaten.

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Everyone wants to be different. Unique. We all want to believe that there is something about us that makes us stand out from others. And though we are all very similar in many ways, we are also individuals. Sure we all want to be successful and happy, but our definition of what success and happiness is varies from person to person. We want the same things, but we want different things.

Being a little bit different from everyone else is actually advantageous. If we were all exactly the same, then there wouldn’t be so much art and creativity in the world. We wouldn’t form relationships as strongly as we do. And we would all be, well, bored. So having your own style and signature is what makes you special. Why, then, do we immediately recoil when who we are bothers other people?

I’m sure you have either been there or you know someone who this happens to often. You know who I’m talking about: the person with a personality that can only be described as polarizing. She’s loud. Opinionated. Unapologetic. And completely herself 100 percent of the time.

Whether you like her or not, there is one thing you can always say about her: she is who she is, and she’s that way all the time. She doesn’t stray from herself for the sake of the comfort of others.

So what does this have to do with you? As women, I think we often play up different aspects of our personality to better ingratiate ourselves in different situations. We are humans, and we are wired to want to be liked by others. But sometimes when we change ourselves to better serve others needs, we bury the things that make us the interesting individual that we are.

When you bury your authentic self, you are depriving people of the greatest gift you have to give: your truth. There is always going to be someone that needs exactly what it is you have to offer. Instead of shrinking, stand taller. Stick to your guns and let go of the fear of standing out in a bad way. Remember: the most important opinion is yours. Are you happy with how you treated someone? How you acted? What you said? Then that’s all that matters.

Action step

It’s easy to be apologetic for who you are when it rubs people the wrong way. Don’t. You’re letting the world down when you fail to give them exactly who you are. We are all very familiar with weaknesses as it’s easy to put them center stage. But being an individual isn’t a weakness; it’s an asset. It can also be a great strength in your life. So focus on that strength and let the world know you’re ready to embrace them. Nothing screams confidence like a woman being comfortable letting her freak flag fly.

Although we administered antibiotic intravenously for 7 days, her white blood cell counts and C-reactive peptide were still high and CT presented that periaortic gas did not reduce. Additionally, it was difficult to alleviate her abdominal pain with analgesics. Rather, the pain worsened day by day. Therefore, we performed abdominal aortic replacement with the rifampicin-bonded gelatin-sealed Dacron graft and omental pedicle grafting. On intraoperative examination, a hard mass was detected in mesentery above the abdominal aortic aneurysm. When incising retroperitoneum, a yellowish abscess was discharged from this mass. Complete debridment could be achieved. Escherichia coli was isolated from aneurysmal tissue and abscess in the mesentery. Postoperatively, intravenous antibiotic had been continued for 4 weeks. After the 4-week antibiotic treatment, postoperative CT showed that gas had disappeared in the mesentery (Figure 2). She was discharged on postoperative day 37 without any complications.

Infective aortic aneurysm is a life-threatening clinical condition, which accounts for <1% of the cases of aortic aneurysm repair and is associated with a high mortality rate.1 Diagnosis of infective aortic aneurysm is based on imaging studies and confirmation that organisms are isolated from blood culture or tissue culture of aneurysmal wall tissue. Blood cultures are positive in 48% of cases, and tissue cultures of infected aorta are positive in 65% of cases.2 The most useful imaging study for diagnosing infected aortic aneurysm is CT. Findings on CT which are highly suspicious for an infected aneurysm include saccular aneurysms, paraaortic soft-tissue mass or fluid, and periaortic gas.3 In our case, it was of interest that periaortic massive gas recognized on CT was presented in mesentery, which was induced by E coli. To our knowledge, such findings have not been reported previously.

The standard treatments of infected aortic aneurysm include antibiotic therapy, surgical interventions, and complete include debridement. In management strategies for infected aortic aneurysm, it is uncertain when the surgical intervention should be performed. In 1 case series, surgical intervention was considered after the infection was controlled in patients responding well to the antibiotic treatment, whereas early surgical intervention was performed in cases of uncontrolled infection. There are no randomized trials guiding the optimal timing when surgical intervention should be performed. It is important to consider serial follow-up CT to decide when we perform surgical intervention for each case.